Bone repair after injury seems to closely resemble embryonic bone development: for example, both processes involve progenitor cell recruitment,vascular network establishment and the differentiation of precursor cells into bone or cartilage. But just how similar are the two processes? To find out,Colnot et al. (see p. 4123) examined fracture repair in the absence of matrix metalloproteinase 9 (MMP9), a key regulator of bone development. They report that the skeletal defects that occur during bone repair in adult Mmp9-/- mice are very similar to those that occur during bone development in these mutants and that, as in development, MMP9 mediates the vascularisation of hypertrophic cartilage. These parallels between endochondral bone formation during development and fracture repair strongly indicate that the embryonic bone differentiation program is reactivated during adult fracture repair.

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